Re: Tinnitus and a dip in the audiogram (Mark Fletcher )

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If I understand you correctly then a problem with this idea is that the med=
ial efferents don't stimulate the outer hair cells and drive more amplifica=
tion=2C but reduce it - the MOC efferents make up a negative feedback loop.
Mark
Date: Tue=2C 11 Sep 2012 10:30:38 -0500
From: flatmax@xxxxxxxx
To: markfletcher22@xxxxxxxx
Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram
=20
=20
=20
=20
Yes I think you are on the right track
...
=20
The link below is an article which discusses emissions in Tinnitus
patients ... I have another link somewhere (can't find it now)
which actually shows spontaneous emissions @xxxxxxxx tinnitus frequencies.
=20
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2170278/pdf/v065p00523.pdf
=20
Matt
=20
On 09/11/2012 10:13 AM=2C Mark Fletcher wrote:
=20
=20
=20
=20
It's an interesting idea. Would you not expect to see evidence
for this in otoacousitc emission work in tinnitus patients (I
don't know if you do or not)?
=20
=20
Mark
=20
> Date: Mon=2C 10 Sep 2012 10:03:24 -0500
> From: flatmax@xxxxxxxx
> Subject: Re: [AUDITORY] Tinnitus and a dip in the
audiogram
> To: AUDITORY@xxxxxxxx
>=20
> Your second point here is one I like. However it may
also be the same as=20
> your first point :)
>=20
> Our mixed-mode Cochlear amplifier supports your
hypothesis.
> http://adsabs.harvard.edu/abs/2011AIPC.1403..611F
>=20
> The general idea is that certain types of Cochlea
damage enhance the=20
> peripheral hearing circuit.
>=20
> For example=2C consider this thought experiment based on
our mixed-mode=20
> Cochlear amplifier model :
>=20
> Imagine that your stereocillia are lopped off in a
small region of inner=20
> hair cells - the same can be said for outer hair cells.
This may happen=20
> due to ageing or damage.
> In this case assume that the stereocillia resistance is
reduced - due to=20
> gaping open ion channels - and ionic currents into the
cell (potassium)=20
> and our from the cell (sodium) are enhanced ... the
hair cell now=20
> experience a depolarisation. This depolarisation
generates more=20
> spontaneous neurotransmitter release.
> The neurotransmitters generate more synaptic
transmission in the=20
> cochlear nerve.
> The cochlear nerve excites the superior olive and this
not only=20
> generates perception of the tone=2C but sends signals
back to the Cochlear=20
> over the lateral and medial efferents.
> The medial efferents stimulate the motors in the outer
hair cells and=20
> they in turn generate movement at the inner hair cells
which start the=20
> process again ... over and over again ... the end
result is a=20
> mecho-neural standing wave ... or 'tinnitus'.
> This type of tinnitus masks low level sound heard
through the ear ...=20
> however if the external sound gets loud enough=2C then it
masks the tinnitus !
>=20
> What do you think ?
>=20
> Matt
>=20
> On 09/10/2012 08:22 AM=2C Matt Winn wrote:
> >
> > Mark and everyone=2C
> >
> > Although I am not a tinnitus researcher=2C I have
had lots of experience=20
> > with patients with tinnitus in the audiology
clinic. Generally=2C we try=20
> > to avoid the confusion of tinnitus with testing
tones by using pulsed=20
> > and/or warbled tones. As you point out=2C this
doesn=92t always work out=20
> > perfectly.
> >
> > It has been my experience that dips in the
audiogram are indeed=20
> > frequently accompanied by tinnitus. having
measuring hearing at the=20
> > VA=2C this connection might be limited to hearing
loss that is=20
> > noise-induced. The two most common explanations I
have heard for this=20
> > are 1) damage to the auditory system at the site
of the hearing loss=20
> > underlies both the threshold elevation and
improper firing by damaged=20
> > nerves=2C and 2) tinnitus that exists in the region
of the dip is not=20
> > masked out by external stimulation because the
external sounds are=20
> > less audible=3B thus rendering tinnitus more
noticeable. This latter=20
> > explanation accounts for the relief from tinnitus
experienced by many=20
> > people who use hearing aids. Specifically=2C
tinnitus isn=92t =93cured=2C=94 but=20
> > it is masked out by the amplified input=2C and then
the tinnitus returns=20
> > after the hearing aid is removed.
> >
> > Returning to the point of tinnitus without
apparent hearing loss=2C I=20
> > have found that salt intake and stress level are
two (among many)=20
> > contributing factors to and my own tinnitus=2C and I
don=92t have hearing=20
> > loss. The dependence of OHCs on metabolic factors
underscores this=20
> > connection=2C which seems anecdotally to be
exacerbated in patients with=20
> > M=E9ni=E8re=92s.
> >
> > Matt
> >
> >
=20
=20
=20
=20
=20
=
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<body class=3D'hmmessage'><div dir=3D'ltr'>
If I understand you correctly then a problem with this idea is that the&nbs=
p=3Bmedial efferents don't stimulate the outer hair cells and drive more am=
plification=2C but reduce it - the MOC efferents make up a <i>negative</i> =
feedback loop.<br><br>Mark<br><br><div><div id=3D"SkyDrivePlaceholder"></di=
v><hr id=3D"stopSpelling">Date: Tue=2C 11 Sep 2012 10:30:38 -0500<br>From: =
flatmax@xxxxxxxx<br>To: markfletcher22@xxxxxxxx<br>Subject: Re: [AUDITORY=
] Tinnitus and a dip in the audiogram<br><br>
=20
=20
=20
=20
<div class=3D"ecxmoz-cite-prefix">Yes I think you are on the right trac=
k
...<br>
<br>
The link below is an article which discusses emissions in Tinnitus
patients ... I have another link somewhere (can't find it now)
which actually shows spontaneous emissions @xxxxxxxx tinnitus frequencies.<br=
>
<br>
<a class=3D"ecxmoz-txt-link-freetext" href=3D"http://www.ncbi.nlm.nih.gov/p=
mc/articles/PMC2170278/pdf/v065p00523.pdf" target=3D"_blank">http://www.ncb=
i.nlm.nih.gov/pmc/articles/PMC2170278/pdf/v065p00523.pdf</a><br>
<br>
Matt<br>
<br>
On 09/11/2012 10:13 AM=2C Mark Fletcher wrote:<br>
</div>
<blockquote cite=3D"mid:BLU162-W20D29ED3BAFEBDAE849621D7930@xxxxxxxx">
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<div dir=3D"ltr">
It's an interesting idea. Would you not expect to see evidence
for this in otoacousitc emission work in tinnitus patients (I
don't know if you do or not)?
<div><br>
</div>
<div>Mark<br>
<br>
<div>&gt=3B Date: Mon=2C 10 Sep 2012 10:03:24 -0500<br>
&gt=3B From: <a class=3D"ecxmoz-txt-link-abbreviated" href=3D"m=
ailto:flatmax@xxxxxxxx">flatmax@xxxxxxxx</a><br>
&gt=3B Subject: Re: [AUDITORY] Tinnitus and a dip in the
audiogram<br>
&gt=3B To: <a class=3D"ecxmoz-txt-link-abbreviated" href=3D"mai=
lto:AUDITORY@xxxxxxxx">AUDITORY@xxxxxxxx</a><br>
&gt=3B <br>
&gt=3B Your second point here is one I like. However it may
also be the same as <br>
&gt=3B your first point :)<br>
&gt=3B <br>
&gt=3B Our mixed-mode Cochlear amplifier supports your
hypothesis.<br>
&gt=3B <a class=3D"ecxmoz-txt-link-freetext" href=3D"http://ads=
abs.harvard.edu/abs/2011AIPC.1403..611F" target=3D"_blank">http://adsabs.ha=
rvard.edu/abs/2011AIPC.1403..611F</a><br>
&gt=3B <br>
&gt=3B The general idea is that certain types of Cochlea
damage enhance the <br>
&gt=3B peripheral hearing circuit.<br>
&gt=3B <br>
&gt=3B For example=2C consider this thought experiment based on
our mixed-mode <br>
&gt=3B Cochlear amplifier model :<br>
&gt=3B <br>
&gt=3B Imagine that your stereocillia are lopped off in a
small region of inner <br>
&gt=3B hair cells - the same can be said for outer hair cells.
This may happen <br>
&gt=3B due to ageing or damage.<br>
&gt=3B In this case assume that the stereocillia resistance is
reduced - due to <br>
&gt=3B gaping open ion channels - and ionic currents into the
cell (potassium) <br>
&gt=3B and our from the cell (sodium) are enhanced ... the
hair cell now <br>
&gt=3B experience a depolarisation. This depolarisation
generates more <br>
&gt=3B spontaneous neurotransmitter release.<br>
&gt=3B The neurotransmitters generate more synaptic
transmission in the <br>
&gt=3B cochlear nerve.<br>
&gt=3B The cochlear nerve excites the superior olive and this
not only <br>
&gt=3B generates perception of the tone=2C but sends signals
back to the Cochlear <br>
&gt=3B over the lateral and medial efferents.<br>
&gt=3B The medial efferents stimulate the motors in the outer
hair cells and <br>
&gt=3B they in turn generate movement at the inner hair cells
which start the <br>
&gt=3B process again ... over and over again ... the end
result is a <br>
&gt=3B mecho-neural standing wave ... or 'tinnitus'.<br>
&gt=3B This type of tinnitus masks low level sound heard
through the ear ... <br>
&gt=3B however if the external sound gets loud enough=2C then i=
t
masks the tinnitus !<br>
&gt=3B <br>
&gt=3B What do you think ?<br>
&gt=3B <br>
&gt=3B Matt<br>
&gt=3B <br>
&gt=3B On 09/10/2012 08:22 AM=2C Matt Winn wrote:<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B Mark and everyone=2C<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B Although I am not a tinnitus researcher=2C I have
had lots of experience <br>
&gt=3B &gt=3B with patients with tinnitus in the audiology
clinic. Generally=2C we try <br>
&gt=3B &gt=3B to avoid the confusion of tinnitus with testing
tones by using pulsed <br>
&gt=3B &gt=3B and/or warbled tones. As you point out=2C this
doesn=92t always work out <br>
&gt=3B &gt=3B perfectly.<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B It has been my experience that dips in the
audiogram are indeed <br>
&gt=3B &gt=3B frequently accompanied by tinnitus. having
measuring hearing at the <br>
&gt=3B &gt=3B VA=2C this connection might be limited to hearing
loss that is <br>
&gt=3B &gt=3B noise-induced. The two most common explanations I
have heard for this <br>
&gt=3B &gt=3B are 1) damage to the auditory system at the site
of the hearing loss <br>
&gt=3B &gt=3B underlies both the threshold elevation and
improper firing by damaged <br>
&gt=3B &gt=3B nerves=2C and 2) tinnitus that exists in the regi=
on
of the dip is not <br>
&gt=3B &gt=3B masked out by external stimulation because the
external sounds are <br>
&gt=3B &gt=3B less audible=3B thus rendering tinnitus more
noticeable. This latter <br>
&gt=3B &gt=3B explanation accounts for the relief from tinnitus
experienced by many <br>
&gt=3B &gt=3B people who use hearing aids. Specifically=2C
tinnitus isn=92t =93cured=2C=94 but <br>
&gt=3B &gt=3B it is masked out by the amplified input=2C and th=
en
the tinnitus returns <br>
&gt=3B &gt=3B after the hearing aid is removed.<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B Returning to the point of tinnitus without
apparent hearing loss=2C I <br>
&gt=3B &gt=3B have found that salt intake and stress level are
two (among many) <br>
&gt=3B &gt=3B contributing factors to and my own tinnitus=2C an=
d I
don=92t have hearing <br>
&gt=3B &gt=3B loss. The dependence of OHCs on metabolic factors
underscores this <br>
&gt=3B &gt=3B connection=2C which seems anecdotally to be
exacerbated in patients with <br>
&gt=3B &gt=3B M=E9ni=E8re=92s.<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B Matt<br>
&gt=3B &gt=3B<br>
&gt=3B &gt=3B<br>
</div>
</div>
</div>
</blockquote>
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